Smith Paul F, Truchet Bruno, Chaillan Franck A, Zheng Yiwen, Besnard Stephane
Department of Pharmacology and Toxicology, School of Biomedical Sciences, Brain Health Research Centre, University of Otago, Dunedin, New Zealand.
Brain Research New Zealand, The Eisdell Moore Centre for Hearing and Balance Research, University of Auckland, Auckland, >New Zealand.
Front Mol Neurosci. 2020 Aug 11;13:140. doi: 10.3389/fnmol.2020.00140. eCollection 2020.
Loss of vestibular function is known to cause spatial memory deficits and hippocampal dysfunction, in terms of impaired place cell firing and abnormal theta rhythm. Based on these results, it has been of interest to determine whether vestibular loss also affects the development and maintenance of long-term potentiation (LTP) in the hippocampus. This article summarizes and critically reviews the studies of hippocampal LTP following a vestibular loss and its relationship to NMDA receptor expression, that have been published to date. Although the available studies indicate that unilateral vestibular loss (UVL) results in reduced hippocampal field potentials in CA1 and the dentate gyrus (DG), the studies involving bilateral vestibular loss (BVL) do not. This may be due to the differences between UVL and BVL or it could be a result of differences. One study reported a decrease in LTP in hippocampal slices following UVL; however, the two available studies have reported different results: either no effect or an increase in EPSP/Population Spike (ES) potentiation. This discrepancy may be due to the different high-frequency stimulation (HFS) paradigms used to induce LTP. The increased ES potentiation following BVL may be related to an increase in synaptic NMDA receptors, possibly increasing the flow of vestibular input coming into CA1, with a loss of selectivity. This might cause increased excitability and synaptic noise, which might lead to a degradation of spatial learning and memory.
已知前庭功能丧失会导致空间记忆缺陷和海马功能障碍，表现为位置细胞放电受损和θ节律异常。基于这些结果，确定前庭丧失是否也会影响海马体中长时程增强（LTP）的发展和维持一直备受关注。本文总结并批判性地回顾了迄今为止已发表的关于前庭丧失后海马体LTP及其与NMDA受体表达关系的研究。尽管现有研究表明单侧前庭丧失（UVL）会导致CA1区和齿状回（DG）的海马场电位降低，但涉及双侧前庭丧失（BVL）的研究却并非如此。这可能是由于UVL和BVL之间的差异，也可能是其他差异导致的结果。一项研究报告称UVL后海马切片中的LTP降低；然而，另外两项现有研究报告了不同的结果：要么没有影响，要么兴奋性突触后电位/群体峰电位（ES）增强。这种差异可能是由于用于诱导LTP的高频刺激（HFS）范式不同。BVL后ES增强增加可能与突触NMDA受体增加有关，这可能会增加进入CA1区的前庭输入流量，同时丧失选择性。这可能会导致兴奋性增加和突触噪声增加，进而可能导致空间学习和记忆能力下降。
